Journal article
Could Alzheimer's Disease Originate in the Periphery and If So How So?
Gerwyn Morris, Michael Berk, Michael Maes, Basant K Puri
MOLECULAR NEUROBIOLOGY | SPRINGER | Published : 2019
Abstract
The classical amyloid cascade model for Alzheimer's disease (AD) has been challenged by several findings. Here, an alternative molecular neurobiological model is proposed. It is shown that the presence of the APOE ε4 allele, altered miRNA expression and epigenetic dysregulation in the promoter region and exon 1 of TREM2, as well as ANK1 hypermethylation and altered levels of histone post-translational methylation leading to increased transcription of TNFA, could variously explain increased levels of peripheral and central inflammation found in AD. In particular, as a result of increased activity of triggering receptor expressed on myeloid cells 2 (TREM-2), the presence of the apolipoprotein ..
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Awarded by NHMRC Senior Principal Research Fellowship
Funding Acknowledgements
MB is supported by a NHMRC Senior Principal Research Fellowship (APP1059660).